Capillary Leak Syndrome

Capillary Leak Syndrome means fluid and proteins leak out of very small blood vessels (capillaries). The fluid moves into the tissues. Blood volume in the vessels drops. Blood pressure can fall to dangerous levels. Albumin (a blood protein) gets low. Red blood cell concentration (hematocrit) goes up because the liquid part of blood is lost. This can cause shock and swelling of many body parts. Episodes may come and go. Some people have warning symptoms 1–2 days before an attack, like tiredness, pain, thirst, or a sudden gain in weight. rarediseases.info.nih.gov+2Cleveland Clinic+2

Capillary leak syndrome (also called systemic capillary leak syndrome, SCLS, or Clarkson disease when idiopathic) is a rare, sudden condition where tiny blood vessels (capillaries) become very “leaky.” Fluid and proteins escape from the bloodstream into tissues. This causes low blood pressure, thickened blood (hemoconcentration), and low blood protein (hypoalbuminemia). Attacks can lead to shock, swelling of arms/legs, kidney injury, and sometimes compartment syndrome. Doctors first rule out more common causes of shock (like infection, bleeding, heart problems) before diagnosing SCLS. Some people have idiopathic SCLS; others develop “secondary” capillary leak with severe infections (sepsis), burns, or certain medications. Monthly IVIG is the best-supported option to prevent idiopathic SCLS flares. PMC+3PMC+3American College of Physicians Journals+3

Doctors often use three “clues” to think about this syndrome. These are: very low blood pressure, high hematocrit (thick blood), and low albumin. There is usually no heavy protein loss in urine. So kidney diseases with heavy protein in urine are less likely. A small number of patients have a monoclonal protein in the blood (MGUS). Attacks can be life-threatening without fast care. JACI Online+2PMC+2

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Other names

People may use different names for this condition:

• Systemic Capillary Leak Syndrome (SCLS).

• Clarkson disease (named after the doctor who first described it).

• Idiopathic Systemic Capillary Leak Syndrome (ISCLS) when no clear cause is found.

• Vascular leak syndrome (often used when drugs like high-dose interleukin-2 cause the leak).
  All of these point to the same core problem: sudden, severe capillary hyper-permeability with shock, hemoconcentration, and hypoalbuminemia. PubMed+1

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Types

You can think about CLS in two broad groups:

1. Idiopathic / Primary (ISCLS or Clarkson disease).
   No clear trigger is found. Attacks are sudden and severe. They have three phases: a prodrome (warning signs), a “leak” phase with low pressure and swelling, and a recovery phase when fluid moves back into the bloodstream. Between attacks, people often feel normal. A monoclonal gammopathy (MGUS) is found in many adults with ISCLS. PubMed+1

2. Secondary CLS (capillary leak as a complication of another problem).
   Here, the capillary leak is due to another disease, infection, injury, or a medicine. Examples include severe infections (like dengue or influenza), sepsis, major burns, pancreatitis, trauma, some cancers, and some cancer or immune medicines (for example high-dose interleukin-2 or newer immune checkpoint medicines). Care focuses on the trigger and on careful fluids, blood pressure support, and close monitoring. Cureus+3PubMed+3Index Copernicus Journals+3

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Causes

Below are common and important causes or triggers. Each short paragraph tells you what it is and how it can lead to capillary leak.

1. Idiopathic (Clarkson disease).
   No outside cause is found. Sudden immune or endothelial changes make capillaries leaky. Attacks repeat. PubMed

2. Sepsis.
   Severe body-wide infection releases many inflammatory signals. These damage the lining of vessels and make them leaky. PubMed

3. Viral infections (general).
   Viruses can injure endothelium and raise cytokines. This raises leak risk. New England Journal of Medicine

4. Dengue virus.
   Dengue can cause a strong inflammatory response. Plasma leaks and shock may follow. Index Copernicus Journals

5. Influenza and other respiratory viruses.
   Cytokine surges and endothelial injury may drive leakage. New England Journal of Medicine

6. COVID-19 cytokine storm.
   Severe immune activation can lead to capillary leak and widespread edema. New England Journal of Medicine

7. Bacterial toxins without full sepsis.
   Some toxins increase permeability even before classic sepsis shows. PubMed

8. Severe allergic reactions (anaphylaxis).
   Histamine and other mediators open capillary junctions and cause fluid escape. PubMed

9. Major burns.
   Heat injury and inflammation break the capillary barrier. Fluid shifts out rapidly. PubMed

10. Acute pancreatitis.
    Pancreatic enzymes and cytokines injure endothelium and increase leak. PubMed

11. Major trauma and crush injury.
    Tissue damage and inflammation increase permeability. PubMed

12. After big surgeries.
    Surgical stress and inflammatory signals may cause transient vascular leak. PubMed

13. High-dose Interleukin-2 therapy (IL-2).
    This cancer therapy can cause “vascular leak syndrome” with hypotension and edema. PubMed

14. Immune checkpoint inhibitors (e.g., pembrolizumab).
    Rare cases of severe capillary leak are reported as immune-related adverse events. Cureus

15. Interferon or other cytokine-based treatments.
    These may tilt immune signals toward leak in rare patients. PubMed

16. Certain chemotherapies (various reports).
    Endothelial injury and cytokines are possible pathways to leak. PubMed

17. Hematologic cancers (e.g., CLL, myeloma).
    Some cases of CLS occur with blood cancers, sometimes alongside MGUS. PMC+1

18. Auto-inflammatory or immune disorders.
    Overactive immune signals can increase permeability. PubMed

19. Toxins and envenomation (selected reports).
    Some exposures harm the endothelium and trigger fluid shift. PubMed

20. Severe systemic inflammation from any cause.
    When many cytokines are released, capillaries can leak even without infection. New England Journal of Medicine

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Symptoms

These are common symptoms and signs. Not everyone has all of them. They can start before, during, or after the main episode.

1. Tiredness and weakness.
   These may begin 1–2 days before an attack (prodrome). Cleveland Clinic

2. Sudden weight gain.
   It comes from fluid moving out of blood vessels into tissues. Cleveland Clinic

3. Muscle aches and body pain.
   These are frequent early clues. Cleveland Clinic

4. Headache and irritability.
   These can occur in the prodrome for some people. Cleveland Clinic

5. Extreme thirst and dry mouth.
   Blood volume drops, so people feel very thirsty. Cleveland Clinic

6. Nausea or abdominal pain.
   The gut can be affected by low blood flow and swelling. Cleveland Clinic

7. Swelling of arms, legs, or whole body (edema).
   Fluid collects in tissues during the leak phase. Cleveland Clinic

8. Very low blood pressure (hypotension).
   This is a key sign and can cause dizziness or fainting. PubMed

9. Dark or low urine (oliguria).
   Kidneys get less blood during shock. Acute kidney injury can follow. BioMed Central

10. Cold, clammy skin, fast heartbeat.
    These are classic shock signs as the body tries to maintain blood flow. PubMed

11. Shortness of breath.
    Later, when fluid returns to the blood, lungs can fill with fluid (pulmonary edema). PubMed

12. Tingling pain in tight muscles (compartment symptoms).
    Severe limb swelling can raise pressure in muscle compartments. malacards.org

13. Confusion or fainting.
    Very low blood pressure reduces brain blood flow. PubMed

14. Chest discomfort.
    Strain on the heart and low pressure can cause symptoms. PubMed

15. Fever or flu-like illness before the attack.
    A recent viral illness often precedes episodes. The New Zealand Medical Journal

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Diagnostic tests

Doctors group testing into five simple buckets. The goal is to confirm leak, measure its effects, find triggers, and exclude other causes like heart failure, severe dehydration, adrenal crisis, or kidney diseases with heavy protein losses.

A) Physical examination (bedside checks)

1. Vital signs with orthostatic blood pressure.
   Low pressure, fast heart rate, and worsening on standing suggest volume loss from capillary leak. PubMed

2. Edema check (pitting vs non-pitting).
   Pressing the skin helps gauge fluid in tissues. Generalized, painful swelling supports leak. malacards.org

3. Jugular venous pressure (JVP) assessment.
   A flat or low JVP suggests low blood volume in vessels, pointing away from heart-failure fluid overload. PubMed

4. Limb circumference and compartment checks.
   Rapid increases and severe pain raise concern for compartment syndrome. malacards.org

B) Manual bedside tests and monitoring

5. Daily (or more frequent) body weight.
   Fast weight gain supports tissue fluid accumulation. Cleveland Clinic

6. Strict fluid balance charting (input vs output).
   This helps judge how much fluid is lost to tissues and guides safe fluid therapy. PubMed

7. Capillary refill time and skin temperature.
   Slow refill and cool skin suggest poor perfusion in shock. PubMed

8. Pulse oximetry.
   Low oxygen can appear during the fluid “return” phase if lungs fill with fluid. PubMed

C) Laboratory and pathological tests

9. Complete blood count (CBC).
   High hematocrit and often high white cells show hemoconcentration during attacks. PubMed

10. Serum albumin and total protein.
    Albumin is low due to leak. This is part of the classic triad with hypotension and hemoconcentration. JACI Online

11. Basic metabolic panel and creatinine.
    Kidney function may worsen in shock. Electrolytes guide treatment. BioMed Central

12. Lactate level.
    High lactate suggests low tissue perfusion from shock. It tracks severity. PubMed

13. Serum protein electrophoresis (SPEP) and immunofixation.
    Many adults with ISCLS have a monoclonal gammopathy (MGUS). Finding this supports the diagnosis. JACI Online

14. Urinalysis with protein quantification.
    Little or no protein in urine helps distinguish CLS from nephrotic syndromes. PubMed

15. Inflammatory markers (CRP, ferritin).
    These often rise with infection or cytokine storms that can trigger leak. New England Journal of Medicine

16. Infection testing (e.g., viral PCRs, cultures) when suspected.
    Identifying dengue, influenza, or bacterial sepsis helps treat the cause in secondary CLS. Index Copernicus Journals

D) Electro-diagnostic and physiologic tests

17. Electrocardiogram (ECG).
    Assesses heart strain during shock, rhythm problems, and guides resuscitation. PubMed

18. Continuous cardiac telemetry and arterial line (in ICU).
    Tracks blood pressure beat-to-beat and helps choose safe fluids and medicines. PubMed

E) Imaging tests

19. Point-of-care ultrasound and echocardiography.
    Helps rule out heart failure, tamponade, or massive pulmonary embolism. IVC collapsibility may show low intravascular volume. PubMed

20. Chest X-ray or CT when needed.
    Early in the leak phase, lungs may look clear. Later, when fluid returns to blood, pulmonary edema can appear. Imaging also helps look for infections or complications. PubMed

Non-pharmacological (therapy/other) measures

1. Early recognition & triage. Teach teams to look for the triad of hypotension + hemoconcentration + hypoalbuminemia without obvious sepsis/bleeding. Rapid recognition lowers time to treatment and complications. PMC+1

2. Careful fluid resuscitation strategy. Start with judicious balanced crystalloids; avoid massive fluid loads when possible because third-spacing is severe in CLS. Reassess frequently. Society of Critical Care Medicine (SCCM)+2PMC+2

3. Early vasopressor support for shock. Use vasopressors when blood pressure stays low after initial fluids; treat shock promptly while avoiding fluid overload. Society of Critical Care Medicine (SCCM)

4. Albumin as an adjunct after large crystalloid volumes. In selected septic-shock/“leaky” states, albumin may help restore intravascular volume when large volumes of crystalloids have already been given. Society of Critical Care Medicine (SCCM)+1

5. Frequent hemodynamic reassessment. Use vitals, urine output, lactate, bedside ultrasound (IVC/cardiac) to guide ongoing fluid/pressors rather than fixed volumes. PMC

6. Monitor for compartment syndromes. Check limb pressures/clinical signs; uncontrolled swelling during the “leak phase” can cause ischemia and requires urgent action. PMC

7. Fasciotomy for limb compartment syndrome (when indicated). If pressures and symptoms confirm true compartment syndrome, urgent surgical decompression prevents nerve/muscle death. AOFAS

8. Abdominal compartment syndrome care. Measure intra-abdominal pressure in refractory shock/oliguria with tense abdomen; follow WSACS algorithms and decompress (surgically) if needed. wsacs.org

9. ICU-level airway/ventilatory support. Intubate if shock, encephalopathy, or respiratory failure develops; ventilatory support buys time while the leak resolves. PMC

10. Renal support. Use early continuous kidney replacement (CRRT) in severe AKI/oliguria with volume overload; it allows fluid removal while maintaining perfusion. PMC

11. ECMO rescue for refractory cardiocirculatory collapse (selected cases). VA-ECMO can bridge patients through extreme shock when standard therapy fails, in expert centers. elso.org+1

12. Thrombosis prevention. When safe, use VTE prophylaxis since hemoconcentration and immobilization raise clot risk (balance against bleeding). PMC

13. Infection evaluation & source control (if secondary CLS suspected). Cultures and source control are essential when sepsis is possible. PMC

14. Meticulous skin & limb care. Elevation, protective padding, and frequent checks help reduce pressure injury in massively edematous limbs. PMC

15. Electrolyte & acid–base management. Replace potassium, magnesium, calcium, and correct acidosis to support heart rhythm and perfusion. PMC

16. Strict input/output and daily weight. Track fluids closely; guide de-resuscitation (diuresis/CRRT) as the “reabsorption phase” starts. PMC

17. Physical therapy & early mobilization during recovery. Prevent deconditioning and joint stiffness once stable. PMC

18. Patient education & action plan (idiopathic SCLS). Teach warning signs, emergency card, and discuss monthly IVIG prevention with a specialist. PMC

19. Avoid triggers when possible. Some flares follow infections or procedures; early treatment of intercurrent illnesses and peri-procedural planning can reduce risk. American Journal of Medicine

20. Multidisciplinary care. Coordinate critical care, nephrology, surgery, hematology/immunology to align fluids, pressors, fasciotomy/ACS decisions, and IVIG plans. PMC+1

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Drug treatments

Important: Except for IVIG (used off-label here for SCLS prevention), most medicines below treat complications of CLS (shock, edema, thrombosis). Indications come from FDA labels; use in CLS may be off-label. Always individualize dosing.

1. Intravenous Immune Globulin (IVIG; e.g., Gamunex-C/Gammagard/Octagam/Panzyga). IVIG monthly (often 1–2 g/kg) is associated with fewer idiopathic SCLS attacks; during acute crises some case series report rapid stabilization. FDA labels cover approved indications (PI, ITP, CIDP, etc.), not SCLS; monitor for thrombosis/renal risk. U.S. Food and Drug Administration+4PMC+4U.S. Food and Drug Administration+4

2. Norepinephrine (first-line vasopressor). Indicated to raise blood pressure in severe acute hypotension; start when hypotension persists after initial fluids, titrate to MAP targets; correct hypovolemia first. FDA Access Data

3. Epinephrine (vasopressor/inotrope). Alternative or add-on vasopressor; label includes hypotension in septic shock; careful titration and weaning are needed. FDA Access Data

4. Vasopressin (add-on vasopressor). For vasodilatory shock refractory to fluids and catecholamines; may reduce catecholamine dose requirements; monitor for decreased cardiac index and hyponatremia. FDA Access Data+1

5. Albumin (Human) 5%/25%. Colloid to help restore intravascular volume in selected patients after substantial crystalloid; watch for volume overload. U.S. Food and Drug Administration+1

6. 0.9% Sodium Chloride & balanced crystalloids (e.g., Lactated Ringer’s). First-line fluids for initial resuscitation; reassess often to avoid harmful edema. FDA Access Data+1

7. Hydrocortisone (IV). Used for refractory shock (stress-dose steroids) per ICU practice; label details dosing and rapid IV use; monitor glucose, infection risk. FDA Access Data

8. Methylprednisolone (IV). Alternative corticosteroid for inflammation/shock; water-soluble succinate salt allows rapid IV administration. FDA Access Data

9. Furosemide (IV). During the “reabsorption phase,” loop diuretics help remove excess fluid once perfusion is restored; monitor electrolytes/renal function. FDA Access Data

10. Heparin (prophylactic/therapeutic anticoagulation). Use when bleeding risk allows, to reduce VTE risk in hemoconcentrated, immobile patients. FDA Access Data

11. Terbutaline (β2-agonist). Historical prophylaxis (with theophylline) in idiopathic SCLS; now largely supplanted by IVIG but sometimes used off-label. Label covers bronchospasm; monitor for tachycardia/arrhythmia. DailyMed

12. Theophylline (methylxanthine). Former prophylaxis partner with terbutaline for SCLS; narrow therapeutic window; today less favored than IVIG. FDA Access Data

13. Tocilizumab (IL-6 receptor blocker). Approved for inflammatory diseases; occasionally tried off-label in cytokine-storm–like capillary leak; monitor LFTs/neutrophils. FDA Access Data

14. Epinephrine IM (anaphylaxis). If capillary leak is precipitated by anaphylaxis, treat per label immediately with IM epinephrine. FDA Access Data

15. Sodium Bicarbonate (IV). For life-threatening acidosis in shock (selected cases); clinician-directed with careful monitoring (label-based use varies by product). FDA Access Data

16. Vasoactive add-ons per ICU protocol (e.g., titrated epinephrine/vasopressin combinations). Used according to shock phenotype and response, with label-guided precautions. FDA Access Data+1

17. Analgesia/sedation (e.g., fentanyl, propofol) to facilitate ventilation/ICU care. Use per label/ICU protocols to lower oxygen demand and ensure ventilator synchrony. PMC

18. Antimicrobials (if infection/sepsis is suspected trigger). Empiric, then targeted therapy per cultures and guidelines; prevents ongoing endothelial injury. PMC

19. Stress-ulcer prophylaxis (e.g., PPI) in the ICU. Prevents GI bleeding in high-risk, intubated, shock patients per ICU standards (label-based use). PMC

20. Electrolyte concentrates (K/Mg/Ca). Corrects dangerous deficits that worsen arrhythmias and hypotension during shock care. PMC

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Dietary molecular supplements

There is no high-quality evidence that specific supplements prevent CLS. Focus remains on medical care and IVIG prevention. The items below are supportive and should be clinician-supervised.

1. Oral rehydration salts during recovery to restore sodium/glucose-coupled water absorption when taking fluids by mouth is safe; not a treatment for acute shock. PMC

2. Protein-adequate diet to rebuild albumin and muscle after the leak resolves (under dietitian guidance). PMC

3. Electrolyte supplements (K/Mg) if low; correct deficits that cause cramps/arrhythmias. PMC

4. Vitamin D if deficient (common in ICU survivors); supports bone/muscle recovery. PMC

5. Thiamine sometimes used in septic shock protocols to support metabolism; clinician-directed only. PMC

6. Omega-3 fatty acids may help general cardiovascular health; not proven for SCLS. PMC

7. Multivitamin during rehabilitation to cover general micronutrient needs after critical illness. PMC

8. Probiotics only if your clinician agrees; avoid in severe immunocompromise. PMC

9. Oral iron only if iron-deficient after hospitalization; monitor labs. PMC

10. Zinc if deficient; limited data in critical illness recovery. PMC

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Immunity-booster/regenerative/stem-cell drugs

There are no FDA-approved stem cell drugs for SCLS. Do not use unproven “stem cell” or “immune booster” products. The options below are immunomodulators with real labels that clinicians sometimes consider for related indications; their use in SCLS is off-label and specialist-only.

1. IVIG (immune globulin). Immune-modulating pooled antibodies; best evidence for preventing idiopathic SCLS flares. Label covers PI/ITP/CIDP; SCLS use is off-label. PMC+1

2. Tocilizumab. IL-6 pathway blocker; used for inflammatory syndromes; limited/experimental for capillary leak physiology. FDA Access Data

3. Corticosteroids (hydrocortisone/methylprednisolone). Temporarily modulate inflammation and catecholamine response in shock care. FDA Access Data+1

4. β2-agonist/theophylline combo (legacy prophylaxis). Historical approach before IVIG became standard; narrow safety window. FDA Access Data

5. ECMO (device, not a drug). For refractory shock with potentially reversible cause; provides temporary circulatory support while the leak resolves. UT Research Information System

6. Avoid unapproved “stem-cell” therapies. FDA warns about unproven stem-cell products outside clinical trials. Discuss only within regulated studies. FDA Access Data

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Surgeries/procedures (why they’re done)

1. Fasciotomy for limb compartment syndrome to relieve dangerous pressure, restore blood flow, and prevent permanent damage. AOFAS

2. Decompressive laparotomy for abdominal compartment syndrome when organ failure and pressures stay high despite medical measures. wsacs.org

3. ECMO cannulation (VA-ECMO) for refractory cardiocirculatory collapse as a bridge to recovery in specialized centers. UT Research Information System

4. CRRT catheter placement to enable continuous dialysis-type therapy for fluid control and kidney support. PMC

5. Airway intubation to secure breathing and allow lung-protective ventilation in shock/respiratory failure. PMC

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Preventions

1. Monthly IVIG prophylaxis (1–2 g/kg). Best evidence to cut relapses and improve survival. PMC

2. Early treatment of infections (common flare triggers). American Journal of Medicine

3. Peri-procedural planning if surgery/anesthesia is needed; coordinate fluids and monitoring. American Journal of Medicine

4. Vaccination per guidelines (after discussing timing with your specialist). U.S. Food and Drug Administration

5. Carry an emergency letter/card explaining SCLS to first responders. American Journal of Medicine

6. Avoid unnecessary large fluid boluses outside monitored settings. Society of Critical Care Medicine (SCCM)

7. Maintain follow-up with an immunology/hematology specialist. jeccm.amegroups.org

8. Recognize personal prodromes (flu-like symptoms, swelling, dizziness) and seek early care. PMC

9. Thrombosis risk reduction (mobility, VTE prophylaxis when appropriate). PMC

10. Healthy recovery plan (nutrition, rehab, sleep) to rebuild reserves. PMC

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When to see a doctor (red flags)

Go immediately to emergency care for fainting, severe dizziness, very low blood pressure, sudden limb swelling, new shortness of breath, chest pain, low urine output, or confusion—especially if you have known SCLS. These are signs of a leak phase and can worsen rapidly without ICU care. PMC

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What to eat and what to avoid

What to eat: Small, frequent meals with enough protein (fish, eggs, legumes, dairy if tolerated) and complex carbs; plenty of fruits/vegetables; and adequate electrolytes as advised by your team. This supports albumin rebuild and muscle recovery once stable. PMC

What to avoid: During the acute leak, do not self-load fluids/salt without medical direction. Later, avoid very salty ultra-processed foods if edema persists; avoid alcohol excess; avoid OTC NSAIDs that may affect kidneys unless your clinician approves. PMC

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FAQs

1. Is CLS the same as sepsis? No. Sepsis can cause leakiness, but idiopathic SCLS has its own pattern; doctors must rule out sepsis and other causes of shock first. PMC

2. What shows up on lab tests? High hemoglobin/hematocrit (thick blood), low albumin, rising lactate/creatinine in shock. PMC

3. How is an attack treated? ICU care with careful fluids, vasopressors, and close monitoring; treat triggers; manage complications. Society of Critical Care Medicine (SCCM)

4. Can IVIG stop attacks? Monthly IVIG reduces relapses in many idiopathic SCLS patients and improves outcomes. PMC

5. Are steroids always used? Steroids are sometimes used in shock or inflammation; practice varies and is individualized. FDA Access Data

6. Why not give lots of fluid quickly? In CLS much of the fluid leaks into tissues, worsening swelling and compartment pressures; use measured, reassessed boluses. PMC

7. What is the “reabsorption phase”? After a day or two, leaked fluid returns to the bloodstream; then clinicians remove excess fluid with diuretics or CRRT. PMC

8. Can medications trigger CLS? Some cancer/immune drugs have been linked to capillary leak; your team will review risks. Cureus

9. Is there a cure? No cure, but prevention (IVIG) and rapid treatment of attacks greatly improve safety. PMC

10. Can children get SCLS? It is rare at any age; diagnosis still relies on the same triad and exclusion of other causes. PMC

11. Will I always need ICU for an attack? Most true attacks require ICU because blood pressure can fall quickly. jeccm.amegroups.org

12. Is ECMO common? No—used only in extreme, refractory shock in experienced centers. UT Research Information System

13. Is there a special diet that prevents SCLS? No proven diet prevents SCLS; medical prevention (IVIG) is key. PMC

14. Can I exercise? Yes, as you recover—gradually and with guidance; stop if you notice swelling or dizziness. PMC

15. Should I avoid vaccines? Discuss timing with your specialist; IVIG can affect some vaccine responses; generally follow recommended immunization with planning. U.S. Food and Drug Administration

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: November 10, 2025.